Research description

Diabetes Research

My research focuses largely on central and peripheral effects of GLP-1, and the regulation of GLP-1 secretion in health and diabetes.

GLP-1 is secreted from intestinal L-cells in response to food intake and stimulates insulin secretion in a glucose dependent manner, while also inhibiting glucagon secretion, reducing appetite and exerting cardioprotective and neuroprotective effects.

GLP-1 based therapy (incretin therapy) is successfully used in the treatment of Type 2 Diabetes (T2D). Ongoing clinical trials also evaluate incretin therapy in subjects with obesity without T2D, as well as in cardiovascular and neurodegenerative disorders. Studies indicate that reduced GLP-1 plasma levels come as a result of diabetes disease progression, and are also associated with increased BMI and insulin resistance independent of T2D. The future of incretin therapy is to understand the mechanisms behind the altered GLP-1 secretion in diabetes in order to learn how to preserve/potentiate endogenous secretion, as well as to identify novel patient groups that may benefit from incretin therapy.

Recent data published by our research group show that the plasma levels of GLP-1 are altered in patients with thoracic aortic aneurysm. Studies designed to identify a potential role for GLP-1 in aneurysm formation are currently ongoing.

Our research group has also shown that saturated fatty acids and simulated diabetic hyperlipidemia induce apoptotic cell death of GLP-1 secreting cells, while unsaturated fatty acids confer lipoprotection, and in a mouse model of insulin resistance a reduced number of intestinal L-cells is indicated.